Search

Innovation in microscopy has often been critical in advancing both fundamental science and technological progress. Notably, the evolution of ultrafast near-field optical nano-spectroscopy and nano-imaging has unlocked the ability to image at spatial scales from nanometers to ångströms and temporal scales from nanoseconds to femtoseconds. This approach revealed a plethora of fascinating light-matter states and quantum phenomena, including various species of polaritons, quantum phases, and complex many-body effects. This review focuses on the working principles and state-of-the-art development of ultrafast tip-enhanced and near-field microscopy, integrating diverse optical pump-probe methods across the terahertz (THz) to ultraviolet (UV) spectral ranges. It highlights their utility in examining a broad range of materials, including two-dimensional (2D), organic molecular, and hybrid materials. The review concludes with a spatio-spectral-temporal comparison of ultrafast nano-imaging techniques, both within already well-defined domains, and offering an outlook on future developments of ultrafast tip-based microscopy and their potential to address a wider range of materials. [ABSTRACT FROM AUTHOR]

Background: Aortic dissection (AD) is a life-threatening cardiovascular emergency and currently lacks effective drug treatment. Inflammation is a critical mechanism in the development of AD, and identifying specific molecular targets to regulate inflammation is crucial for stopping its progression. This study aimed to investigate the role of MR-1 and ROCK1 in the regulation of inflammation in AD and their potentialities as therapeutic targets., Methods: Researchers performed protein immunoblotting on aortic wall tissue from 10 patients who underwent aortic arch replacement and 10 patients who underwent coronary artery bypass grafting to examine the expression levels of MR-1, ROCK1, and inflammatory pathways in the aortas. In vitro experiments, human aortic smooth muscle cells were extracted, and an in vitro dissection model was constructed with angiotensin II. siRNA silencing studies were performed to investigate the effects of MR-1 and ROCK1 on the development of AD and their interconnections., Results: Analysis of aortic tissues revealed significantly elevated levels of MR-1 and ROCK1 in AD patients, and meanwhile the inflammatory indexes showed the same trend. Furthermore, it was observed that overexpression of MR-1 and ROCK1 facilitated smooth muscle cell phenotypic transformation and augmented matrix metalloproteinase release in in vitro settings through inflammatory pathway activation. The relationship between MR-1 and ROCK1 was elucidated, too., Conclusion: MR-1 and ROCK1 overexpression is associated with the occurrence and development of AD through inflammation. This study highlights the role of inflammation in AD development and tap the potentiality of using MR-1 and ROCK1 as targets to alleviate AD development., Competing Interests: The authors report no conflicts of interest in this work., (© 2025 Yin et al.)

Background: Intra-leaflet hemorrhage (IH) plays a well-recognized detrimental role in calcified aortic valve disease (CAVD). However, IH-induced fibro-osteogenic responses in valvular interstitial cells (VICs) appear to be triggered under specific pathological conditions. Iron deficiency (ID), a common co-morbidity in CAVD, may influence these responses. This study investigated the relationship between ID and pathological changes associated with CAVD, and its effects on IH-mediated fibro-osteogenic differentiation of VICs., Methods and Results: Two independent studies were conducted, including 2495 patients in the discovery study and 34 in the validation study. Our data demonstrated that ID was associated with CAVD severity and progression, particularly in an age-dependent manner. Based on these clinical findings, immunofluorescence and Western blot analyses revealed that TFR1, a key iron import transporter, was significantly upregulated in human calcified aortic valves. Concurrently, iron accumulation was detected by Perl's staining in both calcific and non-calcific valve sections. In vitro , VICs cultured with human serum from ID patients showed red blood cell lysis-induced iron overload and fibro-calcific differentiation., Conclusions: ID triggers TFR1-mediated intracellular iron overload, leading to fibrosis and calcification in human VICs, thereby contributing to IH-mediated valve remodeling and calcification. These findings supported the potential role of monitoring and correcting ID to slow or prevent the progression of valvular calcification., (Copyright © 2025 The Author(s). Published by Wolters Kluwer Health, Inc.)